2. LEPROSY
Definition: Leprosy is an infectious chronic
granulomatous disease principally affecting the
skin and peripheral nervous system, caused by
Mycobacterium leprae.
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4. Mycobacterium.leprae is an obligate intracellular
acid-fast gram-positive bacillus with an affinity for
macrophages and Schwann cells, has slow
replication within the Schwann cells, hence the long
incubation period of leprosy.
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5. CAUSES AND PREDISPOSING FACTORS
Humans are the primary reservoir of
Mycobacterium. leprae.
Animal reservoirs of leprosy have been found
in 3 species: 9-banded armadillos,
Chimpanzees, and Mangabey monkeys.
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7. Leprosy is not a highly infectious disease. The
principle means of transmission is by aerosol
spread from infected nasal secretions to exposed
nasal and oral mucosa. Leprosy is not generally
spread by means of direct contact through intact
skin, though close contacts are most vulnerable.
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8. The incubation period is 6 months to 40 years or
longer.
The mean incubation period is 4 years for
tuberculoid leprosy (TT) and 10 years for
lepromatous leprosy (LL).
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9. Most persons are immuned to leprosy. Subclinical disease
is common in endemic areas, and the infection
progresses to clinical disease in only a selected few.
Exposure to nasal discharge of those that remain
untreated for years is thought to be the main cause of
infection.
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10. In addition to exposure to respiratory secretions,
exposure to insect vectors and infected soil has been
suspected as a possible mode of transmission. In
endemic countries, household contacts of patients
are at increased risk for leprosy.
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11. Of particular importance, HIV infection is not a
risk factor for acquiring leprosy, nor does it
increase the clinical symptoms or virulence of
leprosy
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12. INCIDENCE AND PREVALENCE
RACE: Leprosy occurs in all races. African
blacks have a high incidence of the tuberculoid
form of leprosy. People with light skin and
Chinese individuals tend to have the
lepromatous type of leprosy.
Leprosy is endemic in Asia, Africa, the Pacific
basin, and Latin America.
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13. It is more a rural than urban disease.
SEX: In adults, the lepromatous type of
leprosy is more common in men than in
women after puberty, with a male-to-female
ratio of 2:1. In children, the tuberculoid form
predominates, and no sex preference exists.
Women tend to have a delayed presentation,
which increases rates of deformity.
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14. AGE: Leprosy has a bimodal age distribution,
with peaks at ages 10-14 years and 35-44 years.
The disease is rare in infants. Children appear to
be most susceptible to disease and tend to have
the tuberculoid form.
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15. NOTE
ďź Several different approaches for classifying leprosy
exist, but parallels exist.
ďź WHO: paucibacillary and Multibacillary
ďź Further divisions: PAUCIBACILLARY(Tuberculoid âTT
and Borderline tuberculoid BT this is by Ridley-
jopling classification)
ďź MULTIBACILLARY(midborderline or borderline BB)
ďźMULTIBACILLARY( borderline BL and
Lepromatous LL)
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16. CLASSIFICATION
One classification classifies leprosy as either
tuberculoid or lepromatous. These are further
broken down into intermediate or borderline.
Another classification classifies leprosy as
either paucibacillary or multibacillary
depending on the number of lesions and
bacterial index (BI).
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17. PAUCIBACILLARY disease has fewer than 5
lesions and no bacilli on smear testing.
Five or more lesions with or without bacilli is
considered MULTIBACILLARY disease.
IL: This early form causes one to a few
hypopigmentated or sometimes erythematous
macules. Sensory loss is unusual.
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18. TT: Skin lesions are few. One erythematous large
plaque is usually present, with well-defined
borders that are elevated and that slope down
into an atrophic center.
Borderline Tuberculoid leprosy (BT): Lesions in
this form are similar to those in the tuberculoid
form, but they are smaller and more numerous.
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19. Borderline borderline leprosy (BB): Cutaneous
lesions consist of numerous, red, irregularly
shaped plaques that are less well defined than
those in the tuberculoid type.
Borderline lepromatous leprosy (BL): Lesions are
numerous and consist of macules, papules,
plaques, and nodules.
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20. LL: Early cutaneous lesions consist mainly of pale
macules. Late infiltrations are present with
numerous bacilli. Macular lesions are small,
diffuse, and symmetric.
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22. PATHOPHYSIOLOGY
In general, leprosy affects the skin, peripheral
nerves, and eyes. Systemic symptoms may occur.
Specific symptoms vary with the severity of the
disease.
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23. Leprosy commonly affects the superficial
peripheral nerves, skin, mucous membranes of
the upper respiratory tract, anterior chamber of
the eyes, and testes.
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24. Tissue damage depends on the degree to which
cell-mediated immunity is expressed, the type
and extent of bacillary spread and
multiplication, the appearance of tissue-
damaging immunologic complications (i.e. lepra
reactions), and the development of nerve
damage and its sequelae.
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25. The strength of the hostâs immune system
influences the clinical form of the disease. A
strong cell-mediated immunity and a weak
humoral response results in mild forms of
disease, with a few well-defined nerves involved
and lower bacterial loads.
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26. A strong humoral response but relatively absent
cell-mediated immunity results in LL, with
widespread lesions, extensive skin and nerve
involvement, and high bacterial loads.
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27. Therefore, a spectrum of disease exists such that
cell-mediated immunity dominates in mild forms
of leprosy and decreases with increasing clinical
severity. Meanwhile, humoral immunity is
relatively absent in mild disease and increases
with the severity of diseases.
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28. TYPES OF REACTIONS
Leprosy reactions; During the course of
untreated or even treated leprosy, the immune
system may produce inflammatory reactions.
There are two (2) types.
.
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29. Type 1: Results from a spontaneous increase in
cell-mediated immunity.
These reactions can cause fever and
inflammation of the pre-existing skin and
peripheral nerve lesions, resulting in skin
edema, erythema, and tenderness and
worsening nerve functioning.
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30. These reactions particularly if not treated
early contribute significantly to nerve
damage. Because the immune response is
increased, these reactions are termed
reversal reactions, despite the apparent
clinical worsening.
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31. Treatment for type 1: patients with type 1
reaction (except minor skin reaction) are given
Predinisolone 40-60mg per oral once per day
initially, followed by low maintenance dose of as
low as 10-15mg per day for a few months.
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32. Type 2: Also known as Erythema Nodosum
Leprosum or (ENL) are systemic inflammatory
reactions that appear to be a vasculitis or
panniculitis and probably involve circulating
immune complex deposition or increased T-
helper cell function.
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33. Patients may develop erythematous and painful
papules or nodules that may postulate and
ulcerate and cause fever, neuritis,
lymphadenitis, orchitis, arthritis (particularly in
large joints usually knees), and
glomerulonephritis. Hemolytic or bone marrow
suppression may cause anemia, and hepatic
inflammation may cause mild abnormalities in
liver function test.
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34. Treatment for type 2: First and second episodes of
ENL may be treated if mild with Aspirin or, if
significant, with one week of Predinisolone 40-60mg
once per day plus antimicrobials. For recurrent cases
Thalidomide 100-300mg orally once per day.
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35. However because of its teratogenicity,
thalidomide should not be given to women who
may become pregnant.
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36. SIGNS AND SYMPTOMS
Specific Symptoms Vary With The Severity Of
The Disease
Prodromal symptoms are generally so slight that
the disease is not recognized until a cutaneous
eruption is present. However, 90% of patients
have a history of numbness first, sometimes
years before the skin lesions appear.
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37. Temperature is the first sensation that is lost.
Patient cannot sense extremes of hot or cold.
The next sensation lost is light touch, then pain,
and finally deep pressure. These losses are
especially apparent in the hands and feet;
therefore, the chief complaint may be a burning
senastion or ulcer in an anaesthetic extremity.
.
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38. Other parts of the body that might be affected
are the cool areas: superficial peripheral nerves,
anterior chamber of the eyes, testes, chin, malar
eminences, earlobes, and knees.
From this stage, most lesions evolve into the
tuberculoid, borderline, or lepromatous types
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39. Important physical signs generally affect 3
general areas:
ďcutaneous (skin) lesions,
ďneuropathies, and
ďeyes
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40. For cutaneous lesions, assess the number and
distribution of skin lesions. A hypo pigmented
macule with a raised border is often the first
cutaneous lesion. Plaques are also common.
Borderline disease often appears with lesions on
the buttocks.
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41. Regarding neuropathies, assess for areas of hypo
esthesia (light touch, pinprick, temperature and
anhidrosis), especially peripheral nerve trunks
and cutaneous nerves.
The most common nerve affected is the posterior
tibial nerve. Others commonly damaged are the
ulnar, median, lateral popliteal, and facial nerves.
Bedsides sensory loss, there may be associated
tenderness and motor loss.
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42. Eye damage is most often seen with facial lesions.
Lagophthalmos (inability to close the eye), a late
finding in LL, results from involvement of the
zygomatic and temporal branches of the facial
nerve (cranial nerve, CN VII.
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43. Involvement of the ophthalmic branch of the
trigeminal nerve (CN V2) can result in reduced
corneal reflex, leaving dry eyes and reduced
blinking.
Others ;Saddle nose, madarosis
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45. DIAGNOSIS
The diagnosis of leprosy is primarily a clinical
one. Diagnosis was based on 1 of 3 signs:
ďą Hypo pigmented or reddish patches with
definite loss of sensation
ďą Thickened peripheral nerves
ďą Acid-fast bacilli on skin smear or biopsy
material
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46. MANAGEMENT
INVESTIGATIONS
Tissue Smear Testing/Slit-skin Smear (Skin
Biopsy): An incision is made in the skin, and the
scalpel blade is used to obtain fluid from a
lesion. The fluid is placed on a glass slide and
stained by using the Ziehl-neelsen acid-fast
method or the fite method to look for organisms
per 100 bacilli.
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47. Skin smears have specificity but low sensitivity
because 70% of all patients with leprosy have
negative smears. However, this test is useful
because it detects the most infectious patients.
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48. HISTAMINE TESTING: This is used to diagnose
postganglionic nerve injury. Histamine
diphospate is dropped on normal skin and
affected skin, and a pinprick is made through
each site. The site forms a wheal on normal skin
but not where nerve damage is present.
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49. METHACHOLINE SWEAT TESTING: An
intradermal injection of methacholine
demonstrates the absence of sweating in
leprosy lesions. This test is useful in dark-
skinned patients in whom the flare with the
histamine test cannot be seen.
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50. TREATMENT
The management of leprosy includes early
pharmacotherapy and physical, social, and
psychological rehabilitation.
The goals of pharmacotherapy are to stop the
infection, reduce morbidity, prevent
complications and eradicate the disease.
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51. Since 1981, MDT (Multiple drug therapy) has
been advocated by WHO and The USA. MDT
prevents dapsone resistance, quickly reduces
contagiousness, and reduces relapses, reactions,
and disabilities.
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52. TREATMENT PLANS
NON- PHARMACOLOGICAL/ PATIENT
EDUCATION
Patients first need an explanation of the
diagnosis and prognosis. Their fears should be
addressed because of the cultural stigma
associated with leprosy.
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53. The physician should also refute any myths that
the patient may have about leprosy. Patients
may need psychological counseling because they
may have difficulty in coming to terms with the
disease or in feeling rejected by society. The
patient should be reassured that, within a few
days of starting MDT, they are not infectious and
can lead a normal life.
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54. Patients need education about how to deal with
anesthesia of a hand or foot. They must learn to
carefully inspect their extremities for trauma daily.
Patients should also be told to wear proper
footwear and protective equipment as necessary.
Inexpensive canvas shoes with protective insoles
are as effective as special orthopedic shoes.
Inspecting limbs and eyes for onset of anesthesia or
weakness is also important.
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55. Physical therapy and occupational therapy are
important tools in rehabilitation. Patients must
learn how to recognize the onset of lepra reactions,
and they should be told to seek immediate medical
attention if these reactions develop.
Potential deformities can be prevented by
educating patients about how to deal with existing
nerves damage and by treating any sequelae of this
damage.
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56. PHARMACOLOGICAL TREATMENT
The length of treatment ranges from 6
months to 2 years.
Patients are considered non-infectious within 1-
2 weeks of treatment (usually after the first
dose). These drugs are conveniently packaged in
monthly calendar blister packs. Monitor for
drug resistance and adverse reactions to
medications.
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57. Paucibacillary disease can be treated with a
combination of 2 drugs, whereas Multibacillary
disease requires triple-drug therapy.
Single skin lesions (Paucibacillary) can be treated
with a single dose of 3 drugs. The length of
treatment depends on the type of disease and
on the access to drugs.
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58. Current WHO recommendations for
treatment of leprosy are as follows:
Paucibacillary disease: Dapsone 100mg/day plus
rifampicin 600mg once a month for 6 months.
Multibacillary disease: Dapsone 100mg/day plus
rifampicin 600mg once a month plus Clofazimine
300mg once a month and 50mg/day for 1 year.
Single skin lesion: A single dose of rifampicin 600mg,
Ofloxac in 400mg, and Minocycline 100mg. This is
given as single doses
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59. SURGICAL TREAMENT
Emergency surgery may be necessary if a
patient with profound nerve inflammation
presents with a nerve abscess or loss of nerve
function secondary to compression.
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60. Prompt recognition and surgical drainage of the
abscess can often restore nerve function.
Elective surgery may be required for correction
of lagophthalmos (i.e. inability to close the eye).
Reconstructive surgery can be used to repair
nasal collapse in LL.
Other surgery may be needed to improve
function or for cosmesis. Contractures can be
surgically repaired.
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61. COMPLICATIONS
If severe and left untreated; leprosy can cause
clinically significant and debilitating deformity
such as loss of digits.
⢠Lagophthalmos
⢠Madalosis
⢠Saddle nose
⢠Nerve damage
⢠Reversal reactions.
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62. REHABILITATION OF A PATIENT WITH
LEPROSY
Rehabilitation is the important in leprosy
control. Prompt treatment and detection is
important. This may include accessories and
corrective surgical procedures.
Socio-economic and vocational rehabilitation
also forms an integral part in the care of leprosy
patient.
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64. Quiz t/f
1. Toxoplasmosis intermediate host could be a
birds.
2. The cats are the definitive hosts of T. Gondii
3. The period during an epileptic seizure is
referred to as ictal time
4. Toxoplasmosis is a fungal disease
5. Orientation of the patient after an epileptic
attack is not necessary
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